PMID- 1844238
OWN - NLM
STAT- MEDLINE
DCOM- 19930421
LR  - 20211203
VI  - 22
DP  - 1991
TI  - The trk family of oncogenes and neurotrophin receptors.
PG  - 153-70
AB  - To date more than twenty five different oncogenes have been identified in human 
      neoplasias. One of these oncogenes is trk, a transforming gene originally 
      isolated from a colon carcinoma biopsy by using gene transfer assays. This 
      oncogene encodes a chimeric molecule that contains the 221 amino terminal 
      residues of a non-muscle tropomyosin followed by the transmembrane and 
      cytoplasmic domains of the trk proto-oncogene product, a tyrosine protein kinase 
      receptor. trk oncogenes have also been identified in a significant fraction of 
      thyroid papillary carcinomas. Some of these trk oncogenes contain sequences 
      derived from genes other than tropomyosin. One such gene is tpr, a gene first 
      identified as a component of the human met oncogene. The trk proto-oncogene, 
      non-muscle tropomyosin and tpr map in the long arm of chromosome 1. Therefore, 
      trk oncogenes are likely to result from internal rearrangements or from unequal 
      cross-overs between two chromosome 1s. Recent studies have demonstrated that the 
      product of the trk proto-oncogene, gp140trk, is the functional receptor for nerve 
      growth factor (NGF). NGF elicits the rapid phosphorylation of gp140trk on 
      tyrosine residues. Moreover, addition of NGF to NIH3T3 cells expressing gp140trk 
      induces the transient expression of c-Fos, DNA synthesis and morphologic 
      transformation. Finally, transfection of the trk proto-oncogene into NGF 
      non-responsive PC12 mutant cells restores NGF responsiveness. Two additional 
      genes designated trkB and trkC have recently been isolated in our laboratory. 
      These genes are highly related to the trk proto-oncogene and encode tyrosine 
      protein kinases which serve as functional receptors for the NGF-related 
      neurotrophins brain-derived neurotrophic factor (BDNF) and neurotrophic-3 (NT-3), 
      respectively. Whether mutations in these novel members of the trk family of 
      receptor genes are also implicated in human cancer remains to be determined.
FAU - Lamballe, F
AU  - Lamballe F
AD  - Department of Molecular Biology, Bristol-Myers Squibb Pharmaceutical Research 
      Institute, Princeton, New Jersey 08543-4000.
FAU - Klein, R
AU  - Klein R
FAU - Barbacid, M
AU  - Barbacid M
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Princess Takamatsu Symp
JT  - Princess Takamatsu symposia
JID - 9301172
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (MAS1 protein, human)
RN  - 0 (Nerve Growth Factors)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (Neurotrophin 3)
RN  - 0 (Oncogene Proteins)
RN  - 0 (Proto-Oncogene Mas)
RN  - 0 (Proto-Oncogene Proteins)
RN  - 0 (Receptors, Nerve Growth Factor)
RN  - 0 (oncogene protein trk)
RN  - EC 2.7.10.1 (Protein-Tyrosine Kinases)
RN  - EC 2.7.10.1 (Receptor, trkA)
SB  - IM
GS  - trk
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor
MH  - Cell Line
MH  - Gene Expression
MH  - Humans
MH  - *Multigene Family
MH  - Nerve Growth Factors/metabolism
MH  - Nerve Tissue Proteins/metabolism
MH  - Neurotrophin 3
MH  - Oncogene Proteins/*genetics
MH  - *Oncogenes
MH  - Protein-Tyrosine Kinases/*genetics
MH  - Proto-Oncogene Mas
MH  - Proto-Oncogene Proteins/genetics
MH  - *Proto-Oncogenes
MH  - Receptor, trkA
MH  - Receptors, Nerve Growth Factor/*genetics/metabolism
RF  - 60
EDAT- 1991/01/01 00:00
MHDA- 1991/01/01 00:01
CRDT- 1991/01/01 00:00
PHST- 1991/01/01 00:00 [pubmed]
PHST- 1991/01/01 00:01 [medline]
PHST- 1991/01/01 00:00 [entrez]
PST - ppublish
SO  - Princess Takamatsu Symp. 1991;22:153-70.